Search PubMed⌕ Search

Biomedical subjects

C Bismuth

Publications and source records attributed to C Bismuth.

At least 91 records · Page 5Linked to original sources
PubMed1982

[Prolonged high plasma imipramine levels after acute intoxication (author's transl)].

A case of severe intoxication by tricyclic antidepressants with persistence during 14 days of abnormally high plasma imipramine levels is reported. The various factors capable of maintaining plasma imipramine at a high level are discussed. They include mechanical factors (intestinal absorption), ventilation under positive end-expiratory pressure, alterations of hepatic metabolism by other drugs such as metronidazole or cimetidine, and changes in tissue distribution. Attention is drawn to the risks inherent in the various treatments used against acute intoxications and in combined chemotherapy during intensive care generally. When such drugs are necessary, the plasma levels of those with higher toxicity should be monitored.

Adult↗
PubMed1982

[Respective roles of gastric lavage, haemodialysis, haemoperfusion, diuresis and hepatic metabolism in the elimination of a massive meprobamate overdose (author's transl)].

A case of massive meprobamate intoxication (100 g) is reported. On admission, 8 hours later, the plasma meprobamate level was 460 mg/l. The initial shock (hours 8-12) was successfully treated with blood volume expansion and dobutamine. The plasma meprobamate level, which was 340 mg/l when haemodialysis and haemoperfusion were started, fell to 110 mg/l at the end of the treatment. Recovery was uneventful. The amounts of drug eliminated by each method were as follows: (a) gastric lavages at 8 and 26 hours: 66 g; (b) haemodialysis (18-29 hours): 8.5 g; (d) haemoperfusion on Hemopur-charcoal (20-28 hours): 7.5 g (as measured by elution); (e) diuresis (26 hours): 2 g. It may be concluded from these data that sizeable amounts of drug can be extracted by haemodialysis and haemoperfusion, that gastric lavage remains the least invasive and most rewarding method of elimination, and that the role of hepatic metabolism in detoxication has to be taken into account.

Adult↗
PubMed1982

[Beta adrenergic receptor blockade : a self-limited phenomenon explaining the benignancy of acute poisoning with beta adrenergic inhibitors. Report of a series of 40 patients seen at the Fernand-Widal Toxicology Center, with a 0% mortality rate (author's transl)].

Acute poisoning with beta adrenergic inhibitors is rare although such drugs are widely prescribed. Between 1966 and 1980, 40 cases were recorded at the Fernand-Widal Toxicology Center. 40% of patients were asymptomatic and 25% had sinus bradycardia. 35% of patients had specific toxic signs, either atrioventricular block (20%) or hemodynamic disorders (15%); the latter were seen only when associated heart disease was present or when another cardiotropic agent had been absorbed. No deaths were recorded. This favorable prognosis may result from the self-limited nature of poisoning with beta blocking agents, myocardial function being similar to that which follows denervation. In severe cases, management includes pacing and glucagon.

Acute Disease↗
PubMed1982

Prognosis and treatment of paraquat poisoning: a review of 28 cases.

Paraquat poisoning is very severe. When it is ingested, this herbicide may be responsible for causative lesions of the digestive tract, cytolytic hepatitis, renal tubular necrosis, circulatory failure, and/or pulmonary fibrosis. Since a very low dose (as little as one mouthful) is potentially lethal, it is important to understand why 11 of our 28 patients who entered our department for paraquat poisoning survived. The main prognostic factors appear to be the following: Route of administration. Of four patients who had inhaled paraquat aerosols and/or contaminated their skin with the herbicide, all survived. Ingested amount. Above 50 mg/kg, patients died of circulatory failure within 72 h; between 35 and 50 mg/kg, a progressive pulmonary fibrosis occurred. Delay between ingestion and the last meal. Paraquat is adsorbed and neutralized by foodstuffs. Caustic gastric lesions revealed by early endoscopic examination. The occurrence of an organic renal failure. The plasma paraquat concentrations within the first 24 h. Patients whose plasma concentrations do not exceed 2.0, 0.6, 0.3, 0.16, and 0.1 mg/L at 4, 6, 10, 16, and 24 h, respectively, are likely to survive. The different treatments that have been tested (fuller's earth, forced diarrhea, furosemide, hemodialysis, hemoperfusion, artificial ventilation with hypoxic breathing mixtures) did not modify the initial prognosis. The 11 survivals are only linked to the circumstances of the poisonings (route of administration, ingested amount, delay between ingestion and the last meal, etc.). The treatments did not modify the outcome.

Acute Kidney Injury↗
PubMed1982

[Cardiac toxicity of ajmaline. Comparison of acute voluntary poisoning with complications of the ajmaline test].

A comparative and retrospective study of 59 cases of acute voluntary self-poisoning observed at the Toxicology Department of Fernand Widal Hospital, and 15 cases of complications of the Ajmaline test observed in the Cardiology Department of Bichat Hospital showed a similarity in the cardiac effects of high dosage regardless of the mode of administration of the antiarrhythmic. Acute suicidal poisoning in adults or accidental poisoning in children caused toxic effects at doses over more than Ig: they are characterised by their sudden onset after a latent period of 1 to 2 hours and their short duration (no effects after the 12th hour). The ECG changes included:--First degree atrioventricular block (15 p. 100).--Intraventricular conduction defects were observed in almost all cases. They were proportional to the dose taken and were of prognostic interes (no cardiac arrests when the QRS remained less then 0,2 sec).--ST-T wave changes were observed in all patients. They lasted longer and were of no prognostic importance.--Extrasystoles and ventricular tachycardia are nearly always associated with poor hemodynamic tolerance (70 p. 100 of cardiac arrests, compared to only 16 p. 100 in this absence). This intoxication is serious with a mortality of 24 p. 100 of the reported cases and of 9 p. 100 of cases admitted to an Intensive Care Unit.--The complications of the Ajmaline test were similar, the time of apparition being a few minutes instead of a few hours. There were no deaths or serious hemodynamic complications in this series. This is without doubt related to the observation of the contraindications and the fractional administration of the Ajmaline. We conclude that oral Ajmaline, though well tolerated at therapeutic does may cause severe toxic overdose effects. Although its use remains justified in the treatment of arrhythmias, it should not be used for the symptomatic treatment of palpitations and neurovegetative imbalance.

Acute Disease↗
PubMed1982

[Visceral histologic lesions of lethal acute colchicine poisoning. Apropos of 12 cases].

The authors reported histological characteristics (on post-mortem examination) of 12 cases of lethal acute colchicine intoxication and compare these results with the 5 previous anatomical studies of such cases in the literature. Abnormal mitosis (stathmocinesis, "caryomerie", caryorrhexis and mitonecrosis) are constant and essentially seen in the bone marrow and digestive mucosae, especially in oesophagus which squamous epithelium is more resistant to autolysis than others digestive mucosae. Biological or histological symptoms or lesions of intravascular diffuse coagulation are present 7 cases but both biological and histological manifestations in only one case. Hematological disorders are constant when more than 0.5 mg/kg (of corporeal weight) of colchicine has been ingested. Granulocytic elements are most affected both by hypoplasia (essentially in the first four days) and maturation troubles. A microvacuolar non systematized and diffuse liver fatty change is found in 10 cases, probably related to alteration of lipoproteins synthesis and secretion by hepatocytes. Interstitial myocardial oedema is a constant feature; in addition true interstitial myocarditis (with infiltration by polymorphs) is seen in two cases. These cardiac lesions may be related to the cardiogenic shock which is often observed in these patients.

Acute Disease↗
PubMed1981

[Prognostic factors in acute digitalis poisoning (author's transl)].

The prognostic significance of various clinical and biochemical factors was investigated in 179 patients who had absorbed more than 2 mg of digitoxin. The mortality rate in this series was 17%. Supraventricular arrythmias had no influence on prognosis, but the death risk was higher in males and in patients with A-V block. It increased with age, with digitoxin and potassium serum levels and even more with persistent hyperkalemia. Two other factors, previous heart disease and vomiting, were also significant in patients without heart block. Calculated on the basis of 4 clinical factors, the mortality rate varied from 2 to 74%. The death risk in acute digitalis poisoning can therefore be easily assessed from simple clinical criteria.

Acute Disease↗
PubMed1981

Biological evaluation of hemoperfusion in acute poisoning.

The efficiency of hemoperfusion in acute poisoning cannot be clinically estimated, because: (a) concomittant intestinal absorption, hepatic metabolism, and urinary excretion must be taken into account. (b) With supportive treatment alone, spontaneous recovery usually occurs in 98% of the intoxications in Intensive Care Units. The efficiency of hemoperfusion can only be estimated biologically. Measuring the blood level at the beginning and the end of hemoperfusion as well as measuring the clearances of the drug is misleading. A better method is to measure the amount of extracted drug, either indirectly by calculation (from hourly differences of arterio-venous measures of drug concentration multiplied by the blood flow) or directly by elution of the cartridge. In a practical way, if the blood level of drug is readily available after the patient is hospitalized, the optimum efficiency of hemoperfusion can be estimated beforehand, so that the decision to carry out the hemoperfusion can be maintained, postponed, or abandoned. For the most part, the experience of toxicologists has shown hemoperfusion to be ineffective for drugs with weak extracellular distribution (such as Digoxine, tricyclic drugs, heavy metals, Colchicine). Its effectiveness for certain drugs with poor in-vitro dialysance (such as Paracetamol) or with a small percentage of intestinal absorption (such as Paraquat) is still debatable. In the case of intoxications by hypnotic drugs, one hemoperfusion allows an average of 4-12% of the ingested medium and short barbiturates, and 7-17% of the ingested Meprobamate. Whether these results can be judged satisfactory, life-saving, or insignificant is largely a matter of personal standards.

Acute Disease↗
PubMed1981

[Therapeutic attitude in cyanide poisoning (author's transl)].

According to experimental and clinical data, the present treatment of acute cyanide poisoning depends basically on: 1) Dicobaltetracemate in cases of occupational pathology to be given at the working area, to patients with giddiness or mental confusion, 2) Oxygen by assisted ventilation, associated to hydroxocobalamine and sodium thiosulfate, to be administered after admission (patients in coma or circulatory failure). Initial cardio-respiratory arrest requires immediate cardiac massage and assisted ventilation. The rapid cyanide metabolism makes useless the dialysis methods. Frequent complications as metabolic acidosis and acute pulmonary oedema respond to symptomatic treatment. If these therapeutic measures are rapidly applied in confirmed cyanide poisoning, the notion of lethal blood level should be reconsidered. Survivals have been observed with initial plasma levels of 6 mg/l.

Antidotes↗
PubMed1980

[Benzodiazepine physical dependence. 6 cases (author's transl)].

The symptoms include, by ascending order of severity: nightmares and insomnia, nausea and vomiting, muscular weakness or tremor, postural hypotension, hyperthermia, muscle twitching, convulsions, confusional state or psychosis. Prominent features are the late onset of these symptoms, several days after treatment has been discontinued, and the sometimes difficult diagnosis, since patients are usually unaware of their dependence on these drugs. Reinstituting benzodiazepine treatment, then withdrawing it progressively are the best curative measures. Prevention is easy if treatment is gradually rather than abruptly withdrawn in all patients who receive the compound in high dosage for more than one month.

Adult↗